Cholazol H (Alpha-Beta Technology, Worcester, MA), a chemically functionalized, insoluble
dietary fiber with
bile acid sequestrant properties, was studied in 30 male F1 B Golden Syrian hamsters for its effect on plasma
lipid concentrations and early
atherogenesis in experiment 1. In experiment 2, 30 male Golden Syrian hamsters were studied for the effects on plasma
lipids and fecal excretion of
bile acids. In experiment 1, three groups of 10 hamsters each were fed a chow-based hypercholesterolemic diet supplemented with 5%
coconut oil and 0.1%
cholesterol for 6 weeks. After 6 weeks, hamsters were continued on the diet with either 0%
drug (hypercholesterolemic diet [HCD]), 0.5%
cholestyramine (CSTY), or 0.5%
Cholazol H for 8 weeks. Fasting plasma
lipids were measured at weeks 6, 10, and 14, and early
atherosclerosis (fatty streak formation) was measured at week 14. Relative to HCD, CSTY and
Cholazol H significantly lowered plasma total
cholesterol (TC) (-37%, P < .03, and -30%, P < .04, respectively) and plasma very-low and
low-density lipoprotein-cholesterol (nonHDL-C) (-45%, P < .02, and -36%, P < .03, respectively) with no significant effects on plasma HDL-C or
triglycerides (TG). Despite similar reductions in nonHDL-C, only
Cholazol H significantly prevented early
atherosclerosis (-38%, P < .02) relative to HCD. In experiment 2, three groups of 10 hamsters each were fed a chow-based hypercholesterolemic diet supplemented with 10%
coconut oil and 0.05%
cholesterol and either 0%
drug HCD, 0.5% CSTY, or 0.5%
Cholazol H for 4 weeks. Fasting plasma
lipids were measured at weeks 2 and 4, and fecal
bile acids were measured at week 4. Both
Cholazol H and CSTY were equally effective in significantly lowering plasma TC (-16%, P < .003, and -13%, P < .01, respectively) and nonHDL-C (-22%, P < .004, and -18%, P < .02, respectively), with no significant effect on HDL-C and TG relative to HCD.
Cholazol H and CSTY produced a significantly greater concentration of fecal total
bile acids (39%, P < .001, and 28%, P < .002, respectively) relative to HCD. Also, there was a 48% (P < .002) and 65% (P < .001) greater fecal concentration of
cholic acid (CA) for
Cholazol H-treated hamsters compared with HCD- and CSTY-treated hamsters, respectively.
Cholazol H also significantly increased fecal concentration of
deoxycholic acid (DCA; 56%, P < .02) compared with HCD. In summary,
Cholazol H is as effective as CSTY for prevention of diet-induced
hypercholesterolemia and early
atherosclerosis in hamsters.